Effect of Brain Ischemia on Protein Kinase C

Domańska-Janik, Krystyna; Zalewska, Teresa

doi:10.1111/j.1471-4159.1992.tb11360.x

Cited by 76 publications

(25 citation statements)

References 45 publications

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“…There are also serious discrepancies between studies regarding the effect of PKC on the function of the NKCC (27,34,35,38). Tissue-dependent expression of PKC isoforms and isoform-specific response to experimental stimulation and inhibition may have contributed to the controversy regarding regulation of the NKCC by PKC (32,33).…”

Section: Discussionmentioning

confidence: 96%

Protein Kinase C Family Members as a Target for Regulation of Blood–Brain Barrier Na,K,2Cl-Cotransporter During In Vitro Stroke Conditions and Nicotine Exposure

et al. 2006

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Section: Discussionmentioning

confidence: 96%

Protein Kinase C Family Members as a Target for Regulation of Blood–Brain Barrier Na,K,2Cl-Cotransporter During In Vitro Stroke Conditions and Nicotine Exposure

et al. 2006

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“…In vivo experiments utilizing gerbil model of transient ischemia as well as in vitro phorbol stimulation of synaptoneurosomal fraction demonstrate initial PKC activation (translocation) followed by a subsequently enhanced membrane-bound PKC activity (Domanska-Janik and Zalewska, 1992). Pathways involving PKC appear to be involved in ischemiainduced cyclic AMP accumulation by facilitating the postreceptor adenylate cyclase activation (Domanska-Janik and Pylova, 1992).…”

Section: Discussionmentioning

confidence: 99%

mRNA levels of Ca2+-independent forms of protein kinase C in postischemic gerbil brain by Northern blot analysis

Savithiry

Kumar

1994

Molecular and Chemical Neuropathology

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To investigate the role of Ca(2+)-independent forms of protein kinase C (PKC) in ischemic neuronal injury, mRNA expression of PKC was studied by Northern blot analysis. Ischemia was produced in gerbils by 10-min bilateral carotid artery occlusion and was followed by recirculation for 15 min, 6 h, and 24 h. Brains of postischemic and sham-operated animals were removed, forebrains fresh frozen, and processed for Northern blot analysis. Three synthetic oligonucleotide probes based on published cDNA sequences of rat brain PKC for the isozymes delta, epsilon, and zeta were utilized for hybridization. Northern blot analysis showed increased hybridization signal for all three PKC isozymes examined in the 6- and 24-h postischemic groups. Of these, the twofold increases in the expression of PKC delta and zeta were statistically significant in comparison to the control. These results suggest that the mRNA levels of Ca(2+)-independent forms of PKC, in particular, delta and zeta, are temporally stimulated by ischemic injury in the brain and may imply an important role of the enzyme in postischemic neuronal damage. However, since the protein itself was not examined in this study, the significance of the increased expression cannot be ascertained. However, it may reflect a compensatory response to the loss of PKC reported to occur in the reperfusion phase.

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“…19 When the model of cardiac arrest in rats is used, the following occur: in neocortex and hippocampus there is a continuous decrease in PKC activity to approximately 60% of control by 30 minutes of ischemia, and after 11 to 13 minutes of arrest there is no recovery of PKC activity with reperfusion. 18,20,21 When the four-vessel occlusion model in rats is used, the following occur: 5 minutes of ischemia causes no change in PKC activity; 10 minutes of ischemia causes a decrease in hippocampal PKC activity to 65% of control by 2 hours of reperfusion; and 20 minutes of ischemia causes a decrease in hippocampal PKC activity to 40% to 50% of control during ischemia and reperfusion. 22,23 When the twovessel occlusion plus hypotension model in rats is used, the following occur: 15 minutes of ischemia causes a 52% decrease in PKC activity in the membranous fraction of striatum and neocortex during ischemia, 24,25 and 20 minutes of ischemia causes decreases in total PKC activity in hippocampus, cortex, and striatum.…”

Section: Discussionmentioning

confidence: 99%

“…This is consistent with the requirement of ATP for PKC function. When the model of bilateral carotid occlusion in gerbils is used, the following occur: 2 minutes of ischemia causes no PKC activation 16 ; 5 minutes of ischemia causes increased PKC activity in the membranous fraction of CA1 and CA3 hippocampus by 3 days of reperfusion 17 ; 6 minutes of ischemia causes increased PKC activation in CA1 by 1 hour of reperfusion and increased PKC activity in the membranous fraction of hippocampus by 24 hours of reperfusion 16,18 ; and 10 minutes of ischemia causes a decrease in total PKC activity by 2 hours of reperfusion. 19 When the model of cardiac arrest in rats is used, the following occur: in neocortex and hippocampus there is a continuous decrease in PKC activity to approximately 60% of control by 30 minutes of ischemia, and after 11 to 13 minutes of arrest there is no recovery of PKC activity with reperfusion.…”

Section: Discussionmentioning

confidence: 99%

Protein Kinase C Expression and Activity After Global Incomplete Cerebral Ischemia in Dogs

Sieber

Traystman

Brown

et al. 1998

Stroke

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Background and Purpose-Studies suggest that protein kinase C (PKC) activation during ischemia plays an important role in glutamate neurotoxicity and that PKC inhibition may be neuroprotective. We tested the hypothesis that elevations in the biochemical activity and protein expression of Ca 2ϩ -dependent PKC isoforms occur in hippocampus and cerebellum during the period of delayed neurodegeneration after mild brain ischemia. Methods-We used a dog model of 20 minutes of global incomplete ischemia followed by either 6 hours, 1 day, or 7 days of recovery. Changes in PKC expression (Western blotting and immunocytochemistry) and biochemical activity were compared with neuropathology (percent ischemically damaged neurons) by means of hematoxylin and eosin staining. Results-The percentage of ischemically damaged neurons increased from 13Ϯ4% to 52Ϯ10% in CA1 and 24Ϯ11% to 69Ϯ6% in cerebellar Purkinje cells from 1 to 7 days, respectively. The occurrence of neuronal injury was accompanied by sustained increases in PKC activity (240% and 211% of control in hippocampus and cerebellum, respectively) and increased protein phosphorylation as detected by proteins containing phosphoserine residues. By Western blotting, the membrane-enriched fraction showed postischemic changes in protein expression with increases of 146Ϯ64% of control in hippocampal PKC␣ and increases of 138Ϯ38% of control in cerebellar PKC␣, but no changes in PKC␤ and PKC␥ were observed. By immunocytochemistry, the neuropil of CA1 and CA4 in hippocampus and the radial glia in the molecular layer of cerebellum showed increased PKC␣ expression after ischemia. Conclusions-This study shows that during the period of progressive ischemic neurodegeneration there are regionally specific increases in PKC activity, isoform-specific increases in membrane-associated PKC, and elevated protein phosphorylation at serine sites.

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Effect of Brain Ischemia on Protein Kinase C

Cited by 76 publications

References 45 publications

Protein Kinase C Family Members as a Target for Regulation of Blood–Brain Barrier Na,K,2Cl-Cotransporter During In Vitro Stroke Conditions and Nicotine Exposure

Protein Kinase C Family Members as a Target for Regulation of Blood–Brain Barrier Na,K,2Cl-Cotransporter During In Vitro Stroke Conditions and Nicotine Exposure

mRNA levels of Ca2+-independent forms of protein kinase C in postischemic gerbil brain by Northern blot analysis

Protein Kinase C Expression and Activity After Global Incomplete Cerebral Ischemia in Dogs

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